Adenosine triphosphate–dependent potassium channel modulation and cardioplegia- induced protection of human atrial muscle in an in vitro model of myocardial.

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Adenosine triphosphate–dependent potassium channel modulation and cardioplegia- induced protection of human atrial muscle in an in vitro model of myocardial stunning  Francesco Monti, MD, Katsunori Iwashiro, MD, Sandra Picard, PhD, Anna Criniti, PhD, Saverio La Francesca, MD, Giovanni Ruvolo, MD, Ugo Papalia, MD, Pietro Paolo Campa, MD, Benedetto Marino, MD, Paolo Emilio Puddu, MD  The Journal of Thoracic and Cardiovascular Surgery  Volume 119, Issue 4, Pages 842-848 (April 2000) DOI: 10.1016/S0022-5223(00)70022-5 Copyright © 2000 American Association for Thoracic Surgery Terms and Conditions

Fig. 1 Experimental protocol for investigation of protective effects of normothermic (37°C) cardioplegia (STHS), either alone or associated with KATP channel modulators, on human atrial trabeculae in an in vitro model of myocardial stunning. FF relationships were studied after each different experimental phase. Hypoxia was performed at a high pacing rate (400-ms CL). The Journal of Thoracic and Cardiovascular Surgery 2000 119, 842-848DOI: (10.1016/S0022-5223(00)70022-5) Copyright © 2000 American Association for Thoracic Surgery Terms and Conditions

Fig. 2 Effects of hypoxia-reoxygenation and dobutamine challenge on human atrial contractility. DT variations are expressed as means ± SEM. P values refer to ANOVA for repeated measures performed for the 4 hypoxia-related groups: control, STHS, STHS plus bimakalim, and STHS plus glibenclamide. TRCs are included for visual comparative purposes. Note highly significant P values for group (G), time (T) and group · time (G*T) factors. Note marked positive inotropic action of dobutamine in preparations subjected to cardioplegic arrest, either alone or in the presence of 100 nmol/L bimakalim, whereas 1 μmol/L glibenclamide inhibited protective effects of cardioplegia after hypoxia. The Journal of Thoracic and Cardiovascular Surgery 2000 119, 842-848DOI: (10.1016/S0022-5223(00)70022-5) Copyright © 2000 American Association for Thoracic Surgery Terms and Conditions

Fig. 3 Changes of velocity of tension developed by human atrial trabeculae after hypoxia-reoxygenation and dobutamine challenge. Values of log[velocity of DT] are expressed as means ± SEM. For comparison, 95% confidence intervals of basal values for all 54 preparations included in the randomized study are shown in gray. A, *P < .05 and **P < .01 versus control, Student t test with Bonferroni correction. Note that 100 nmol/L bimakalim added to cardioplegic solution significantly improved the velocity of DT after hypoxia-reoxygenation and dobutamine challenge. B, *P < .05 and **P < .005 versus base, Student t test for paired data. Note that velocity of DT was decreased after dobutamine challenge when 1 μmol/L glibenclamide was associated with cardioplegia, and conversely it was improved in the STHS plus bimakalim group (P < .05, Fisher exact test). The Journal of Thoracic and Cardiovascular Surgery 2000 119, 842-848DOI: (10.1016/S0022-5223(00)70022-5) Copyright © 2000 American Association for Thoracic Surgery Terms and Conditions

Fig. 4 Changes in FF relationships of human atrial trabeculae after reoxygenation (A) and dobutamine challenge (B) in control and STHS-related groups. Developed tension variation (%DT) of DT measured during basal FF at corresponding cycle length is expressed as means ± SEM. P values refer to ANOVA for repeated measures performed for the 4 groups. Note higher FF-related developed tension variation after cardioplegic treatment, either alone or in the presence of 100 nmol/L bimakalim, than in the control and STHS plus glibenclamide groups, which fits with improved human atrial contractility, as illustrated in Fig 2. Note that the protective effect of STHS plus bimakalim after reoxygenation disappeared at the high pacing rate (A) , whereas after dobutamine treatment (B) , there was no such interference. The Journal of Thoracic and Cardiovascular Surgery 2000 119, 842-848DOI: (10.1016/S0022-5223(00)70022-5) Copyright © 2000 American Association for Thoracic Surgery Terms and Conditions